Related Experiment Video
Updated: Mar 23, 2026
Hypoxia Alters miRNAs Levels Involved in Non-Mendelian Inheritance of Autism Spectrum Disorder in Mice
Published on: July 11, 2025
Maternal hypomagnesemia alters renal function but does not program changes in the cardiovascular physiology of adult
R N Schlegel1, K M Moritz1, T M Paravicini1
11School of Biomedical Sciences,The University of Queensland,Brisbane,QLD,Australia.
Insights
Maternal magnesium deficiency during pregnancy did not lead to long-term cardiovascular or renal issues in offspring mice. Adult offspring showed no programmed hypertension or reduced nephron number despite altered magnesium excretion.
Area of Science:
- Developmental Biology
- Nutritional Science
- Cardiovascular Physiology
Background:
- Maternal undernutrition negatively impacts fetal development, increasing risks for later-life cardiovascular and renal diseases.
- Infants born small for gestational age often develop hypertension and reduced glomerular number.
- The long-term health effects of maternal magnesium (Mg2+) deficiency on offspring are largely unknown.
Purpose of the Study:
- To investigate the long-term cardiovascular and renal consequences in adult offspring following maternal dietary Mg2+ deficiency during pregnancy.
- To determine if maternal Mg2+ deficiency programs for hypertension or renal abnormalities in offspring.
Main Methods:
- A mouse model was used to induce dietary Mg2+ deficiency in pregnant mothers.
- Cardiovascular function (mean arterial pressure, heart rate, stress responses) was assessed in adult offspring (6 months) via radiotelemetry.
- Renal outcomes, including nephron number, urine flow, and Mg2+ excretion, were evaluated in offspring.
Main Results:
- No significant differences were observed in 24-h mean arterial pressure, heart rate, or cardiovascular stress responses between offspring of Mg2+-deficient mothers and controls.
- Nephron number was similar in both groups.
- Offspring from Mg2+-deficient mothers exhibited increased urine flow and, in males, reduced Mg2+ excretion.
Conclusions:
- Moderate maternal dietary Mg2+ deficiency during pregnancy did not result in programmed hypertension or a nephron deficit in adult offspring mice.
- The study suggests no long-term adverse cardiovascular health outcomes for offspring exposed to maternal Mg2+ deficiency.
- Altered urinary Mg2+ excretion in offspring indicates potential subtle, long-term metabolic adaptations.
Abstract:
Maternal undernutrition is known to adversely impact fetal health and development. Insults experienced in utero alter development of the fetus as it adapts to microenvironment stressors, leading to growth restriction and subsequent low birth weight. Infants born small for gestational age have significantly increased risk of developing cardiovascular and renal disease in later life, an effect that is often characterized by hypertension and reduced glomerular number. Maternal magnesium (Mg2+) deficiency during pregnancy impairs fetal growth, however, the long-term health consequences for the offspring remain unknown. Here, we used a mouse model of dietary Mg2+ deficiency before and during pregnancy to investigate cardiovascular and renal outcomes in male and female adult offspring at 6 months of age. There were no differences between groups in 24-h mean arterial pressure or heart rate as measured by radiotelemetry. Cardiovascular responses to aversive (restraint, dirty cage switch) and non-aversive (feeding response) stressors were also similar in all groups. There were no differences in nephron number, however, Mg2+-deficient offspring had increased urine flow (in both males and females) and reduced Mg2+ excretion (in males only). Despite evidence suggesting that maternal nutrient restriction programs for hypertension in adult offspring, we found that a moderate level of maternal dietary Mg2+ deficiency did not program for a nephron deficit, or alter cardiovascular function at 6 months of age. These data suggest there are no long-term adverse outcomes for the cardiovascular health of offspring of Mg2+ deficient mothers.
Related Concept Videos
01:07Teratogenicity
01:33Hormonal Regulation